Major endogenous reactive oxygen species (ROS) result from electron leakage through electron transport in mitochondria (Cadenas, E. et al., (2000) Free. Radic. Biol. Med. 29, 222-230; Lenaz, G. (2001) IUBMB Life. 52, 159-164; Chen, Q. et al., (2003) J. Biol. Chem. 278, 36027-36031; Turrens, J. F. (1997) Biosci. Rep. 17, 3-8; and Liu, S. S. (1999) J. Bioenerg. Biomembr. 31, 367-376). It is believed that excessive ROS results in induction of apoptosis or cancer (Jacobson, M. D. (1996) Trends. Biochem. Sci. 21, 83-86; Mignotte, B. et al., (1998) Eur. J. Biochem. 252, 1-15; Floyd, R. A. (1990) FASEB J. 4, 2587-2597; Cerutti, P. A. et al., (1991) Cancer Cell. 3, 1-7; and Kovacic, P et al., (2001) Curr. Med. Chem. 8, 773-796), but direct evidence is somewhat lacking. Many researchers who study oxidative stress resort to either the chemical production of ROS in cells using drugs such as paraquat (Hassan, H. M. et al., (1979) J. Biol. Chem. 254, 10846-10852; and Feng, J. et al., (2001) Dev. Cell. 1, 633-644) or the use of electron transport inhibitors so as to increase endogenous production of free radicals (Aitken, R. J. et al., (1997) Mol. Reprod. Dev. 47, 468-482; and Saybasili, H. et al., (2001) Antioxid. Redox. Signal. 3, 1099-1104). However, these drugs also pose severe cellular toxicity and therefore such studies may not provide accurate portrayals of the deleterious effects of natural endogenous ROS from mitochondria. So as to avoid this pitfall, the present inventors have previously isolated a mutant of C. elegans, mev-1 (kn1) (Ishii, N. et al., (1990) Mutat. Res. 237, 165-171), which has a genetic dysfunction in electron transport and therefore overproduces ROS in its mitochondria (Senoo-Matsuda, et al., (2001) J. Biol. Chem. 276, 41553-41558). This gene encodes Cyt-1, which is homologous to SDHC in humans and is one subunit of complex II (Ishii, N. et al., (1998) Nature 394, 694-697). The kn1 mutation leads to apoptosis and precocious aging in C. elegans (Senoo-Matsuda, et al., (2003) J. Biol. Chem. 278, 22031-22036; Honda, S, et al., (1993) J. Gerontol. 48. B57-61; and Hosokawa, H. et al., (1994) Mech. Ageing. Dev. 74, 161-170).